Pathways Linking Socioeconomic Status and Postpartum Smoking Relapse

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Pathways Linking Socioeconomic Status and Postpartum Smoking Relapse Michael S. Businelle a , Darla E. Kendzor a , Lorraine R. Reitzel b , Jennifer Irvin Vidrine b , Yessenia Castro b , Patricia Dolan Mullen c , Mary M. Velasquez d , Ludmila Cofta-Woerpel e , Paul M. Cinciripini e , Anthony J. Greisinger f , and David W. Wetter b a Division of Health Promotion and Behavioral Sciences, University of Texas School of Public Health, Dallas, TX, USA b Department of Health Disparities Research, University of Texas M.D. Anderson Cancer Center, Houston, TX, USA c Division of Health Promotion and Behavioral Sciences, University of Texas School of Public Health, Houston, TX, USA d Center for Social Work Research, University of Texas at Austin, Austin, TX, USA e Department of Behavioral Science, University of Texas M.D. Anderson Cancer Center, Houston, TX, USA f Kelsey Research Foundation, Houston, TX, USA Abstract Background—Low socioeconomic status (SES) exacerbates the high rate of smoking relapse in women following childbirth. Purpose—This study examined multiple models of potential mechanisms linking SES and postpartum smoking relapse among women who quit smoking due to pregnancy. Methods—Participants were 251 women enrolled in a randomized clinical trial of a new postpartum smoking relapse prevention intervention. Four models of the prepartum mechanisms linking SES and postpartum smoking relapse were evaluated using a latent variable modeling approach. Results—Each of the hypothesized models were a good fit for the data. As hypothesized, SES indirectly influenced postpartum smoking relapse through increased prepartum negative affect/ stress, reduced sense of agency, and increased craving for cigarettes. However, the model that included craving as the sole final pathway between SES and relapse demonstrated superior fit when compared with all other models. Conclusions—Findings have implications for future interventions that aim to reduce postpartum relapse. Keywords Smoking; Postpartum; Structural Equation Modeling; Relapse; Socioeconomic Status Corresponding Author: Michael S. Businelle, Ph.D., University of Texas School of Public Health, Dallas Regional Campus, 6011 Harry Hines Blvd., V8.112, Dallas, TX, 75390-9128, [email protected] Phone: 214-648-1070. Conflict of Interest Statement: The authors have no conflict of interest to disclose. NIH Public Access Author Manuscript Ann Behav Med. Author manuscript; available in PMC 2014 April 01. Published in final edited form as: Ann Behav Med. 2013 April ; 45(2): . doi:10.1007/s12160-012-9434-x. NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author Manuscript

Transcript of Pathways Linking Socioeconomic Status and Postpartum Smoking Relapse

Pathways Linking Socioeconomic Status and PostpartumSmoking Relapse

Michael S. Businellea, Darla E. Kendzora, Lorraine R. Reitzelb, Jennifer Irvin Vidrineb,Yessenia Castrob, Patricia Dolan Mullenc, Mary M. Velasquezd, Ludmila Cofta-Woerpele,Paul M. Cinciripinie, Anthony J. Greisingerf, and David W. Wetterb

aDivision of Health Promotion and Behavioral Sciences, University of Texas School of PublicHealth, Dallas, TX, USAbDepartment of Health Disparities Research, University of Texas M.D. Anderson Cancer Center,Houston, TX, USAcDivision of Health Promotion and Behavioral Sciences, University of Texas School of PublicHealth, Houston, TX, USAdCenter for Social Work Research, University of Texas at Austin, Austin, TX, USAeDepartment of Behavioral Science, University of Texas M.D. Anderson Cancer Center, Houston,TX, USAfKelsey Research Foundation, Houston, TX, USA

AbstractBackground—Low socioeconomic status (SES) exacerbates the high rate of smoking relapse inwomen following childbirth.

Purpose—This study examined multiple models of potential mechanisms linking SES andpostpartum smoking relapse among women who quit smoking due to pregnancy.

Methods—Participants were 251 women enrolled in a randomized clinical trial of a newpostpartum smoking relapse prevention intervention. Four models of the prepartum mechanismslinking SES and postpartum smoking relapse were evaluated using a latent variable modelingapproach.

Results—Each of the hypothesized models were a good fit for the data. As hypothesized, SESindirectly influenced postpartum smoking relapse through increased prepartum negative affect/stress, reduced sense of agency, and increased craving for cigarettes. However, the model thatincluded craving as the sole final pathway between SES and relapse demonstrated superior fitwhen compared with all other models.

Conclusions—Findings have implications for future interventions that aim to reduce postpartumrelapse.

KeywordsSmoking; Postpartum; Structural Equation Modeling; Relapse; Socioeconomic Status

Corresponding Author: Michael S. Businelle, Ph.D., University of Texas School of Public Health, Dallas Regional Campus, 6011Harry Hines Blvd., V8.112, Dallas, TX, 75390-9128, [email protected] Phone: 214-648-1070.

Conflict of Interest Statement: The authors have no conflict of interest to disclose.

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Published in final edited form as:Ann Behav Med. 2013 April ; 45(2): . doi:10.1007/s12160-012-9434-x.

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IntroductionAlthough the number of women who smoke cigarettes in the United States has declined overthe past half century [1], approximately 22% of all women of child bearing age continue tosmoke [2] and 10–12% of women report smoking during their pregnancy [3]. Although halfof all women who smoke quit immediately prior to or during their pregnancy [4, 5], up to80% of those women will return to smoking within one year postpartum [e.g., 6].Unfortunately, many studies have shown that children exposed to secondhand smoke havehigher mortality rates and are at greater risk for numerous health problems includingrespiratory diseases and ear infections [e.g., 7, 8, 9]. In order improve the health of womenand their children, studies are needed to illuminate the reasons why women return tosmoking during the postpartum period.

Low socioeconomic status (SES) has been consistently linked with higher rates of smokingin women before and during pregnancy [e.g., 10, 11–15] and is also a risk factor for relapseto smoking following childbirth [10, 13, 16]. Despite widespread knowledge of the relationsbetween SES, smoking, and smoking relapse, few studies have examined the mechanismslinking SES to postpartum smoking relapse in women who quit due to pregnancy. However,women of lower SES experience higher levels of perceived stress and negative affect duringpregnancy compared to their higher SES counterparts [17, 18]. Higher perceived stress andnegative affect are related to lower self-efficacy for abstinence [17] and a higher likelihoodof postpartum relapse [e.g., 16, 19, 20]. Finally, abstinent pregnant women who report loweragency (e.g., self-efficacy/confidence) for maintaining abstinence are more likely to relapsepostpartum [21, 22]. Thus, increased negative affect and perceived stress, and lower self-efficacy for smoking cessation may tax the already limited resources of socioeconomicallydisadvantaged pregnant women and may trigger greater craving for cigarettes andpostpartum smoking relapse. The purpose of this study was to investigate prepartumnegative affect/stress, self-efficacy, and craving as potential mechanisms linking SES andpostpartum smoking relapse.

Over the past decade, a number of conceptual models have been developed that link SES tospecific health behaviors and overall health. Notable models include those developed byGallo and Mathews [23] and Adler and Ostrove [24]. Both of these models hypothesize thatSES is linked to health and health behavior through environmental and psychosocialvariables. More specifically, these models hypothesize that individuals of lower SES mayexhibit more negative health behaviors than individuals of higher SES due to increasedexposure to stressors and fewer interpersonal and intrapersonal resources that can be used toeffectively cope with perceived stressors. Recent research has provided support for thesemodels by indicating that perceived stress, negative emotions (e.g., depression, anxiety),social support, and other interpersonal and intrapersonal resources and constraints domediate the relation between SES and several health behaviors [e.g., 25, 26]. Thesemediating variables may be particularly relevant for pregnant women, given the stressassociated with pregnancy and caring for a newborn (e.g., physical discomfort, sleepdeprivation, decreased availability of time to care for self and others), pregnancy-related andpostpartum negative affect, and the increased need for social support and other inter- andintra-personal resources in the pre- and postpartum periods (e.g., assistance with prenatalcare, postpartum care of the newborn, effective coping skills)[e.g., 17, 18, 27]. Perceivedstress and negative emotions may be exacerbated among socioeconomically disadvantagedpregnant women who have fewer financial and social resources, and this may increase thelikelihood of postpartum relapse.

In the area of substance abuse, the Witkiewitz and Marlatt [28] cognitive-behavioral modelalso hypothesizes mediational pathways through which distal variables like SES can affect

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substance use and relapse. More specifically, variables such as negative affect, perceivedstress, cognitions, social support, agency (e.g., self-efficacy for quitting), and craving arehypothesized to play key roles in the relation between SES and substance use. Notably,Witkiewitz and Marlatt [28] hypothesized reciprocal relationships among cognitive variables(e.g., agency, expectancies, craving, motivation), affective variables, and stress-relatedvariables. In other words, craving for nicotine may increase negative affect and vice versa,with either direction of causality affecting the likelihood of relapse. These relationshipsremain to be evaluated among socioeconomically disadvantaged pregnant women who mayexperience both elevated negative affect and craving.

Based on the work of Adler and Ostrove [24], Gallo and Mathews [23], and Witkiewitz andMarlatt [28], Businelle and colleagues [29] developed and tested a conceptual modelevaluating the hypothesized mediational pathways linking SES to smoking cessation in aracially/ethnically diverse sample of men and women seeking smoking cessation treatment.Results indicated that low SES increased the likelihood of relapse through its effects onperceived neighborhood disadvantage, social support, negative affect/stress, and agency forquitting. Additionally, results showed that craving indirectly increased the likelihood ofrelapse by increasing negative affect and perceived stress, and by reducing agency.

Importantly, many of the significant pathways described in Businelle et al. [29] have yet tobe tested in women who quit smoking due to pregnancy. For instance, it is unclear whetherprepartum craving for cigarettes predicts postpartum relapse among women who have beenabstinent for an extended period of time, although previous studies have indicated thatcraving significantly predicts relapse among ex-smokers even after extended periods ofabstinence [e.g., 30, 31]. Additionally, it is unclear if the pattern of relationships betweennegative affect, perceived stress, agency, and craving in women who quit smoking due topregnancy mirrors the pattern seen in the sample described in Businelle et al. [29].

The primary purpose of this study was to evaluate conceptual models of the pathwayslinking SES and postpartum smoking relapse in a sample of women who quit smoking dueto pregnancy. Key potential mediators were previously selected based on relevant theoreticalmodels [e.g., 24, 28, 32] and hypothesized models were developed in which theconfiguration of several key latent variables and the direction of pathways between latentvariables were based on the model described in Businelle et al. [29; see Figure 1, Model 1].Specifically, low SES was hypothesized to be related to high negative affect/stress, which inturn was hypothesized to result in lower agency, which was hypothesized to increase thelikelihood of postpartum smoking relapse. In addition, this model included hypothesizedindirect pathways linking craving to smoking relapse through high negative affect and lowagency. Because the model described in Businelle et al. [29] was developed in asubstantially different sample of smokers (i.e., a racially/ethnically diverse sample of currentsmokers attempting to quit); a secondary purpose of this study was to determine if alternateconfigurations of the hypothesized mediating variables and the inclusion of additionalpathways between the mediators and subsequent relapse would significantly improve themodel fit for this unique sample. Specifically, we proposed three alternate models to:determine whether craving for cigarettes was a more proximal predictor for postpartumrelapse as compared to agency (see Figure 1, Model 2); test whether including directpathways from negative affect/stress and craving to relapse would improve the fit of Model1 (see Figure 1, Model 3); and determine if adding direct pathways from negative affect/stress and agency to relapse would improve the fit of Model 2 (see Figure 1, Model 4).

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MethodsParticipants

Data for the current study were collected as part of a randomized clinical trial designed toevaluate a Motivation And Problem Solving (MAPS) counseling approach to preventpostpartum relapse among women who quit smoking due to pregnancy [33]. Participantswere recruited through the local health care system and via newspaper, radio, bus, and clinicadvertisements. Participants were eligible to participate if they: 1) were at least 18 years ofage, 2) were fluent in English, 3) were between 30 and 33 weeks pregnant, and 4) quitsmoking during their current pregnancy or within 2 months prior to becoming pregnant.

ProceduresPotential participants were screened over the telephone to determine eligibility. Those whomet the study inclusion criteria were invited to enroll in the study over the phone and werescheduled for the baseline session. Informed consent was completed at the baseline session.Participants were randomly assigned to receive usual care (n = 115) or one of twoexperimental MAPS treatments (n =136). Those assigned to the usual care group receivedself-help materials and brief relapse prevention advice in the clinic after they completedbaseline questionnaires. Materials used for usual care were based on the Treating TobaccoUse and Dependence Clinical Practice Guideline [34]. Participants assigned to the MAPSgroups received usual care and either six MAPS telephone counseling sessions or six MAPStelephone counseling sessions and two in-person MAPS sessions [see 33 for further detailsabout the MAPS treatment sessions]. All demographic and psychosocial measures describedbelow were collected during the baseline visit which occurred between 30 to 33 weeks ofpregnancy. Participants completed follow-up assessments at 8 and 26 weeks postpartum.Participants were compensated with $40.00 gift cards and other small items (e.g., diaperbags) at each assessment visit. Participant enrollment and flow through the study have beenreported elsewhere [see 33]. The study was approved by the Institutional Review Board ofthe University of Texas MD Anderson Cancer Center.

MeasuresDemographics—Demographic information including age, annual household income, totalyears of education completed, number of prior pregnancies, partner status (i.e., married orliving with significant other = 1; single = 0), race/ethnicity (i.e., three dummy codedvariables representing African American, Latino, and Other Race were created with Whiteas the comparison group), and employment status (i.e., employed or on maternity leave froma full- or part-time job = 1; homemaker, student, or unemployed = 0) were collected at thebaseline visit.

Tobacco use—Information related to tobacco use was collected at the baseline visit andincluded years smoked and pre-pregnancy smoking rate.

Negative Affect/stress—Negative affect/stress was assessed using three separatemeasures collected at the prepartum baseline visit. Variables were chosen and combinedbased on the findings of previous research [e.g., 29]. The Positive and Negative Affect Scale[PANAS; 35] consists of Positive Affect and Negative Affect subscales, each consisting of10 affect related adjectives. Scores range from 10 to 50 and higher scores indicate higherlevels of positive and negative affect. Only the Negative Affect subscale was used in thecurrent study. The Center for Epidemiologic Studies Depression Scale [CES-D; 36] consistsof 20-items designed to assess depressive symptoms in community populations. Scoresrange from 0 to 60, and scores 16 and higher indicate clinically significant distress. The

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Perceived Stress Scale [37] consists of four items designed to assess the degree to which anindividual believes his/her life is stressful. Scores range from 0 to 16 and higher scoresindicate greater levels of perceived stress.

Agency—Two measures of prepartum agency were administered during the baseline visitin the current study. The Self-Efficacy/Confidence Scale [SECS; 38] was developed to assessan individual’s confidence in their ability to refrain from smoking in three types ofsituations: positive affect/social situations, negative affect situations, and habit/cravingsituations. Each subscale consists of three items and higher scores indicate higherconfidence in the ability to refrain from smoking. The Affective Information ProcessingQuestionnaire [AIPQ; 39] assesses an individual’s belief in his/her ability to control theirmood without smoking in 10 negative affect laden hypothetical situations. Higher scoresindicate greater belief in the ability to successfully control mood without smoking.

Craving—Craving for cigarettes was assessed at the baseline visit using the four itemCraving subscale from the Wisconsin Smoking Withdrawal Scale [WSWS; 40]. Each item israted on a 5-point Likert-type scale, with higher scores indicating higher levels of craving.

Smoking Status—Self-reported postpartum smoking abstinence (i.e., continuouslyabstinent = 0; smoking at least one puff by follow-up = 1) was assessed at the week 8 andweek 26 follow-up sessions and was confirmed via carbon monoxide (CO) readings or bysalivary cotinine in cases where we could not obtain CO readings. CO readings greater thanor equal to 10 parts per million were considered indicative of relapse as were salivarycotinine readings greater than or equal to 20 ng/ml.

Analytic PlanThe Mplus software package [41] was used to fit the data to the four hypothesized structuralequation models. Potential mediator variables were selected based upon previous researchand hypothesized links between SES and smoking relapse [e.g., 25, 29, 42]. Latent variableswere created for SES, Negative Affect/Stress, Agency, and Craving. The factors used toconstruct these latent variables were identical to those used in Businelle et al. [29].Specifically, the SES latent variable included three indicators: education, income, andemployment status. The Negative Affect/Stress latent variable included the Positive andNegative Affect Scale negative affect scale, the Perceived Stress Scale, and the Center forEpidemiologic Studies Depression Scale. The Agency latent variable included the threeSelf-Efficacy/Confidence Scale subscales and the Affective Information ProcessingQuestionnaire. The Craving latent variable was made up of the four-item Craving subscalefrom the Wisconsin Smoking Withdrawal Scale. Age, partner status, race/ethnicity, andnumber of previous births, were included as covariates in all models. In order to control forthe effect of treatment on relapse status, a treatment group variable (i.e., Motivation AndProblem Solving [MAPS] vs. usual care) was included in all models. The primary outcomevariable was whether or not participants relapsed by the 8 week postpartum follow-up. Incases where abstinence status could not be determined due to missing data, participants wereconsidered relapsed consistent with the “intent-to-treat” approach commonly used in othersmoking cessation studies [e.g., 43, 44]. However, analyses were also conducted aftercoding those who did not attend the 8 week follow-up session as missing.

Employment status, partner status, race/ethnicity, and relapse status were coded ascategorical variables. All other variables were coded as continuous. The outcome variablefor all models was categorical. As such, weighted least squares with robust standard errors(WLSMV) parameter estimation was used to estimate free parameters. The followinggoodness of fit indices were used to determine how well the observed data fit the

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hypothesized models [see 45, 46–48]: 1) chi-square goodness of fit index [e.g., 46, 49], 2)comparative fit index [CFI; 45], 3) Tucker-Lewis Index [TLI; 50], 4) root mean square errorof approximation [RMSEA; 51], and 5) weighted root mean square residual (WRMR).Recommended cutoff points for these indices are as follows: CFI ≥ .95, TLI ≥ .95, RMSEA≤ .05, and WRMR ≤ 1.0. Significance of indirect pathways between SES and relapse statuswere tested using the “Model Indirect” command in Mplus.

As previously noted, four structural equation models were developed and tested todetermine: 1) if the current data were a good fit for the model described in Businelle et al.[29], and 2) if alternate models of the relation between SES, psychosocial mediators, andpostpartum smoking relapse would fit the current data better than the Businelle et al. model.Although all of the tested models included the same observed and latent variables, thelinkages of the latent variables differed across the models (see Figure 1). Model 1 was mostclosely related to the previously tested model [29]. Alternate models were compared toModel 1 to determine the best fitting model for the current data.

Because there are no empirical tests of the superiority of non-nested structural equationmodels using the WLSMV estimator, models were re-estimated using the maximumlikelihood estimator in order to obtain the Bayesian Information Criterion [BIC; 52] for eachmodel. The BIC is a likelihood measure that can be used to determine if one non-nestedstructural equation model is superior to another [52–54]. Specifically, BIC differences ofgreater than 10 points may be interpreted as “very strong” evidence that the model with thesmaller BIC is superior to the model with the larger BIC [53, 54]. BIC differences of 6–10points indicate “strong” evidence that the model with the smaller BIC is superior to themodel with the larger BIC [53, 54].

ResultsParticipant Characteristics

A total of 251 women enrolled in the study (32% African American, 30% Latino, 36%White). On average, participants were 24.6 (±5.3) years old and reported 12.9 (±2.0) yearsof education. Overall, participants reported 0.88 previous births (±1.14) and 62.8% of thesample reported that they were married or living with their significant other. Medianhousehold income was $20,000 – $29,999 and 41% percent of the sample reported that theywere currently working or on maternity leave from a full or part time job. Participantsreported smoking 10.2 (±7.6) cigarettes per day prior to becoming pregnant and had beensmoking for 6.8 (±4.3) years. Consistent with recent abstinence from smoking, expiredcarbon monoxide levels were 2.1 (±1.6) parts per million on average at the baseline visit.See Table 1 for additional participant characteristics.

AttritionA total of 200 (79.7%) participants completed assessments at the 8-week follow-up and 197(78.5%) participants completed the 26-week follow-up. Participants who did not completefollow-up assessments were coded as relapsed. A total of 64.5% and 80.1% of the samplewere classified as relapsed by the 8-week and 26-week follow-ups, respectively.

Associations among Observed VariablesZero order correlations among all observed variables are listed in Table 2. As expected,variables within the same latent construct had the highest correlations. Notably, week 8relapse status was significantly correlated with all but two of the indicator variables (i.e.,income and PANAS negative affect) that were included in the models tested in this study.

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Structural Equation ModelingFour models were developed to describe possible relations between SES and week 8 relapseafter controlling for age, partner status, race/ethnicity, and number of previous births.Results indicated that Model 1 was a good fit for the observed data: χ2 (43, N = 251) =54.59, p = .11; CFI = .959; TLI = .967; RMSEA = .033; WRMR = .832 and examination ofthe LaGrange modification indices resulted in no changes to the model. Results indicatedthat Model 2 [χ2 (45, N = 251) = 53.90, p = .17; CFI = .969; TLI = .975; RMSEA = .028;WRMR = .799], Model 3 [χ2 (43, N = 251) = 49.59, p = .23; CFI = .977; TLI = .981;RMSEA = .025; WRMR = .785], and Model 4 [χ2 (44, N = 251) = 53.08, p = .16; CFI = .968; TLI = .974; RMSEA = .029; WRMR = .794] were also an adequate fit for the observeddata. It is notable that each of the hypothesized direct pathways in Models 1 and 2 weresignificant. However, the direct pathways linking the Negative affect/Stress and Agencylatent variables to relapse were not significant in Models 3 and 4 (i.e., only the directpathway from Craving to relapse was significant). Each of these models was re-run aftercoding women who did not attend the week 8 follow up as missing. Results were virtuallyidentical to the intent to treat analyses.

In order to determine if any of the alternate models were superior to Model 1 [from 29],Bayesian Information Criterion (BIC) values for each model were obtained by refitting thedata using maximum likelihood estimation. Results revealed that the BIC for Model 1 was15520.94, the BIC for Model 2 was 15509.92, the BIC for Model 3 was 15518.26, and theBIC for Model 4 was 15518.63. Thus, based on the Raftery [54] criteria, these findingsindicate that there is “very strong” evidence that Model 2 is superior to Model 1 and“strong” evidence that Model 2 is superior to Models 3 and 4. Since Models 3 and 4 werenot significantly different from Model 1, they will not be discussed further. The standardizedpath coefficients and factor loadings for Models 1 and 2 are displayed in Figures 2 and 3respectively. BIC values were also obtained by re-running these maximum likelihoodmodels after coding women who did not attend the week 8 follow up as missing (i.e.,completer only analyses). Results indicated that there is “strong” evidence that Model 2 issuperior to Models 1, 3, and 4.

SES directly and indirectly influenced week 8 postpartum relapse status. Specifically, lowSES was significantly related to greater risk of relapse by the 8 week follow-up assessmentacross all models. The indirect pathways between SES and week 8 relapse status wereexamined using the “Model Indirect” function in Mplus. Results indicated that the indirectpathway linking SES to relapse in Model 1 (i.e., SES → Negative Affect/Stress → Agency→ Week 8 Postpartum Relapse) approached significance (standardized structural coefficient= −0.024, p = .057). In Model 2, both of the indirect paths linking SES to week 8 smokingrelapse were significant. Specifically, the path SES → Negative Affect/Stress → Agency →Craving → Week 8 Postpartum Relapse was significant (standardized structural coefficient= −.018; p = .02) and the path SES → Negative Affect/Stress → Craving → Week 8Postpartum Relapse was also significant (standardized structural coefficient = −.023; p = .03). Importantly, negative affect/stress, craving, and agency also had significant direct/indirect effects on relapse status in both Model 1 and Model 2. A decomposition of all theindirect and total effects on relapse status for Models 1 and 2 for each of the latent variablesis depicted in Table 3.

Models were rerun using the Week 26 data. Each of the models were a good fit for the Week26 relapse data, and there were only minor differences between the Week 8 and Week 26models. For example, with respect to our final model, the only difference between the Week8 and the Week 26 model was that the pathway between treatment group and relapse statusbecame nonsignificant in the Week 26 model.

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Other IssuesMost previous studies have shown that nicotine dependence is related to SES [e.g., 55, 56]and smoking cessation [e.g., 16, 57, 58], although several recent studies have indicated thatlevel of nicotine dependence may not predict smoking relapse [e.g., 29, 59]. In addition,studies have found that living with a smoker may predict smoking relapse in women whoquit smoking due to pregnancy [e.g., 22, 60, 61]. In the current study, multiple measures ofnicotine dependence (i.e., number of cigarettes smoked per day prior to pregnancy, time tofirst cigarette after waking prior to pregnancy) and living with a smoker were related to SESindicators, but were not related to postpartum smoking relapse. Attempts to add thesevariables into the tested models resulted in reductions in model fit. Therefore, thesevariables were not included in final models.

DiscussionThe current study is among the first to examine mediational pathways between SES andpostpartum smoking relapse in women who quit smoking due to pregnancy. As mostpostpartum smoking relapse occurs among socioeconomically disadvantaged women [4],understanding the mechanisms that underlie this process may inform relapse preventioninterventions that aim to reduce relapse rates within vulnerable postpartum populations.Multiple mediator variables (i.e., negative affect/stress, craving, and agency) were examinedand four plausible models were tested. Analyses indicated that a model that included cravingas the sole final pathway between SES and relapse (Model 2) was the best fit for the data. Asshown in Figure 3, low SES both directly and indirectly increased the likelihood of relapsein women who quit smoking due to pregnancy. Specifically, findings indicated that womenof lower SES reported higher levels of negative affect/stress during the latter part of theirpregnancy (i.e., 30–33 weeks into pregnancy) and both high negative affect/stress and lowagency increased the likelihood of postpartum relapse by increasing craving to smoke. Thesefindings illuminate mechanisms through which SES impacts postpartum smoking relapseand highlight potential targets for future tailored treatments to prevent postpartum relapse.

The superiority of Model 2 over the other three models that were tested in the current studyhighlights the important role that prepartum craving plays as a mediator of the SES-postpartum relapse relationship. To the best of our knowledge, this is the first study to showthat prepartum craving predicts postpartum relapse. However, some previous work hasindicated that craving for cigarettes can predict smoking relapse, long after cessation [30,31]. The weight of the relationship between craving and postpartum relapse becomes moreevident when the results of Models 3 and 4 are taken into consideration. In Models 3 and 4,direct pathways linking each of the cognitive variables (i.e., negative affect/stress, agency,and craving) to smoking relapse were simultaneously tested. Results indicated that the pathsbetween craving and relapse maintained significance, while pathways between the othercognitive variables and relapse were not significant. These findings suggest that prepartumnegative affect/stress and agency primarily have an indirect impact on postpartum smokingrelapse through their effects on prepartum craving. Although smoking cessation treatmentsmost definitely have a major component focused on coping with craving, there are actuallyvery few relapse prevention interventions that are implemented outside the context ofachieving initial cessation. Perhaps even more importantly, coping with craving is not aprimary topic of focus for smokers who have been abstinent for extended periods of time asare women who quit smoking immediately prior to or during pregnancy [see 62 for a reviewon pre and postpartum smoking interventions]. Therefore, the fact that prepartum craving forcigarettes is the final common pathway linking SES to smoking relapse suggests thatinterventions may need to have a specific focus on preparing women, and low SES womenin particular, to cope with cravings for cigarettes, and that high levels of prepartum cravingmight signal a need for intervention or additional intervention. In addition, low SES women

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may benefit from additional training in learning how to diffuse negative affect/stress andlow self-efficacy for quitting before they can lead to greater cravings for cigarettes andeventual relapse.

The results of this study support findings from previous research that have shown therelation between SES and smoking relapse is mediated by negative affect/stress [29, 63],craving [29], and agency [29, 63]. However, this is the first study to simultaneously examinemultiple mediational pathways between SES and postpartum smoking relapse. It isimportant to note that the models tested in the current study examined how affective andcognitive variables may interact to effect the relation between SES and postpartum relapse,whereas the Adler and Ostrove (1999), Gallo and Matthews (2003), and Witkiewitz andMarlatt (2004) models are more general frameworks of the relation between SES and health/health behavior. Thus, this study has begun to clarify how SES interacts with theseimportant mechanisms to increase the likelihood of postpartum relapse. Future researchshould examine whether these models can be improved by adding other potential mediatorsof the SES-relapse relationship (e.g., health concern, knowledge of the negative healtheffects of cigarette smoke on children, biological measures of stress, neighborhooddisadvantage, infant temperament, sleep quantity/quality).

It is notable that a previous study found that agency was the best fitting final commonpathway between SES and smoking relapse and craving only influenced relapse indirectlythrough increased negative affect/stress and reduced agency [29]. The finding that agencywas not the best fitting final common pathway in the current study was not completelyunexpected considering the significant differences between the samples described inBusinelle et al. [29] and the current study. For instance, the Businelle et al. [29] sampleconsisted of men and women who were undergoing a quit attempt and the negative affect/stress, agency, and craving measures were all collected on the quit date. In this study, thesevariables were collected 30–33 weeks into pregnancy, months after subjects had already quitsmoking. Taken together, these findings suggest that post-quit cravings measured shortlybefore childbirth have a more direct impact on postpartum relapse than negative affect/stressand agency, while quit date measures of agency have a more direct impact on relapse in menand women during the early stages of a quit attempt. One potential explanation is thatcraving experienced months after quitting serves as a critical marker of relapse vulnerability.For example, craving may reflect a host of potential influences (e.g., dependence, co-morbidity, chronic stress, environmental factors). Conversely, among individuals who are intheir first days of abstinence, craving is a much more typical experience and may be lesspredictive than one’s confidence that they can maintain abstinence [e.g., see 29].

The current study has a number of strengths. First, the models tested in the current studywere based on a smoking relapse model that was developed in a completely different sampleof diverse smokers seeking cessation treatment [see 29]. Thus, there is evidence that thisgeneral framework may be applied to diverse groups of smokers/former smokers seekingtreatment. Second, the current sample was comprised of a diverse group of women (e.g.,nearly identical numbers of African American, Latino, and White women). Thus, studyfindings may be generalizable across several racial/ethnic groups. A third strength of thecurrent study is that self-reported abstinence was confirmed via biochemical means at bothpostpartum time points. A final strength is that multiple models were tested and compared todetermine the best fitting model for the current data. Future research should further test thesemodels to determine if Model 2 is in fact superior to the other three models of the relationbetween SES and postpartum smoking relapse.

The current study also has a number of limitations. First, although each of the four testedmodels were an adequate fit for the observed data and validate portions of a previously

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tested model [29], other plausible models may have been an equal or better fit for the data.Thus, additional evaluation of these models using larger sample sizes is needed for furthermodel validation [64]. A second limitation is that the mediating variables (i.e., craving,negative affect/stress, agency) were all collected at the same point in time. Future researchstudies should collect longitudinal data on each hypothesized mediator variable in order toobtain a more accurate indication of the temporal interactions between each of thehypothesized mediator variables. The timing of assessments has important implications forthe results of the current study. Assessments of negative affect/stress, agency, and cravingwere conducted at 30–33 weeks into pregnancy, while relapse was measured at 8 and 26weeks postpartum. Future studies should build upon this model by adding postpartumassessments of these key mechanisms. Postpartum assessments could be used in conjunctionwith prepartum assessments to identify whether the trajectories of these variables predictrelapse. A third limitation of the current study is that negative affect, depression, andperceived stress were all placed into one latent construct. This was done because thesevariables were highly correlated (range of correlation: .518 to .655) and each of them loadedhighly onto the Negative Affect/Stress latent variable (loadings ranged from .682 to .819).Future research in this area may benefit from collecting larger samples sizes that will allowfor the parsing of the roles of perceived stress, negative affect, and depression as mediatorsof the SES-smoking relapse relation.

The findings of this study highlight potential avenues through which the SES-postpartumsmoking relapse gradient may be reduced. Specifically, prepartum interventions forsocioeconomically disadvantaged women who quit smoking due to pregnancy may be moreeffective if they target variables that mediate the SES-relapse relationship (e.g., negativeaffect/stress, agency for maintaining abstinence, and craving for smoking). Suchinterventions might be more effective than standard cessation interventions because theywould specifically address and ameliorate the varying stressors and circumstances thatcontribute to postpartum relapse. Although the appropriate timing of such tailoredtreatments (i.e., prepartum, postpartum, or both) is unclear, previous researchers havesuggested that relapse prevention treatments may be most beneficial if they are offeredthrough the prenatal and postpartum periods [e.g., 6, 65]. Future research studies shouldfurther examine how specific sources of perceived stress and negative affect (e.g., financialstrain, temperament of the child, lack of transportation, neighborhood disadvantage) impactsmoking craving and subsequent relapse in low SES women. Clarification of how specificpre- and post-partum stressors impact craving and relapse may lead to the development ofmore effective postpartum relapse prevention treatments. In addition, postpartumpharmacotherapy may be considered as a way to reduce craving and negative mood for lowSES women who quit smoking due to pregnancy.

AcknowledgmentsThis manuscript was supported by grants from the National Cancer Institute (R01CA89350 to DWW;R25TCA57730 to MSB and DEK), the American Cancer Society (MRSGT-12-114-01-CPPB to MSB,MRSGT-10-104-01-CPHPS to DEK), and the CDC (K01DP001120 to LRR; K01DP000086 to JIV). This researchwas also supported in part by the National Institutes of Health through MD Anderson's Cancer Center SupportGrant CA016672.

References1. Giovino, GA.; Chaloupka, FJ.; Hartman, AM., et al. Cigarette Smoking Prevalence and Policies in

the 50 States: An Era of Change – The Robert Wood Johnson Foundation ImpacTeen TobaccoChart Book. Buffalo, NY: University at Buffalo, State University of New York; 2009.

2. Centers for Disease Control and Prevention. Smoking prevalence among women of reporductive age- United States. Morbidity & Mortality Weekly Report. 2006; 57:849–852.

Businelle et al. Page 10

Ann Behav Med. Author manuscript; available in PMC 2014 April 01.

NIH

-PA Author Manuscript

NIH

-PA Author Manuscript

NIH

-PA Author Manuscript

3. Martin JA, Hamilton BE, Sutton PD, et al. Births: Final data for 2004. National Vital StatisticsReports. 2006; 55:1–101.

4. Tong VT, Jones JR, Dietz PM, D'Angelo D, Bombard JM. Trends in smoking before, during, andafter pregnancy - Pregnancy risk assessment monitoring system (PRAMS), United States, 31 sites,2000–2005. Morbidity and Mortality Weekly Report. 2009; 58:1–29. [PubMed: 19145219]

5. Colman GJ, Joyce T. Trends in smoking before, during, and after pregnancy in ten states. AmericanJournal of Preventive Medicine. 2003; 24:29–35. [PubMed: 12554021]

6. Mullen PD. How can more smoking suspension during pregnancy become lifelong abstinence?Lessons learned about predictors, interventions, and gaps in our accumulated knowledge. Nicotine& Tobacco Research. 2004; 6:S217–S238. [PubMed: 15203823]

7. DiFranza JR, Aligne CA, Weitzman M. Prenatal and postnatal environmental tobacco smokeexposure and children’s health. Pediatrics. 2004; 113:1007–1015. [PubMed: 15060193]

8. Jedrychowski W, Flak E. Maternal Smoking during Pregnancy and Postnatal Exposure toEnvironmental Tobacco Smoke as Predisposition Factors to Acute Respiratory Infections.Environmental Health Perspectives. 1997; 105:302–306. [PubMed: 9171991]

9. U.S. Department of Health and Human Services. The Health Consequences of Involuntary Exposureto Tobacco Smoke: A Report of the Surgeon General. Atlanta, GA: U.S. Department of Health andHuman Services, Centers for Disease Control and Prevention, Coordinating Center for HealthPromotion, National Center for Chronic Disease Prevention and Health Promotion, Office onSmoking and Health; 2006.

10. Kahn RS, Certain L, Whitaker RC. A Reexamination of Smoking Before, During, and AfterPregnancy. American Journal of Public Health. 2002; 92:1801–1808. [PubMed: 12406812]

11. Fingerhut LA, Kleinman JC, Kendrick JS. Smoking before, during, and after pregnancy. AmericanJournal of Public Health. 1990; 80:541–544. [PubMed: 2327529]

12. McKnight A, Merret JD. Smoking in pregnancy - a haelth education problem. Journal of the RoyalCollege of General Practitioners. 1986; 36:161–164. [PubMed: 3735200]

13. Nafstad P, Botten G, Hagen J. Partner's smoking: A major determinant for changes in women'ssmoking behaviour during and after pregnancy. Public Health. 1996; 110:379–385. [PubMed:8979756]

14. Centers for Disease Control and Prevention. Trends in Smoking Before, During, and AfterPregnancy — Pregnancy Risk Assessment Monitoring System (PRAMS), United States, 31 Sites,2000– 2005. Morbidity & Mortality Weekly Report. 2009; 58:1–36. [PubMed: 19145219]

15. Centers for Disease Control and Prevention. Cigarette Smoking Among Adults and Trends inSmoking Cessation - United States, 2008. Morbidity & Mortality Weekly Report. 2009; 58:1227–1232. [PubMed: 19910909]

16. Higgins ST, Heil SH, Badger GJ, et al. Educational disadvantage and cigarette smoking duringpregnancy. Drug and Alcohol Dependence. 2009; 104:S100–S105. [PubMed: 19442460]

17. Crittenden KS, Manfredi C, Cho YI, Dolecek TA. Smoking cessation processes in low-SESwomen: The impact of time-varying pregnancy status, health care messages, stress, and healthconcerns. Addictive Behaviors. 2007; 32:1347–1366. [PubMed: 17097815]

18. Rutter DR, Quine L. Inequalities in pregnancy outcome: A review of psychosocial and behaviouralmediators. Social Science & Medicine. 1990; 30:553–568. [PubMed: 2408152]

19. Park ER, Chang Y, Quinn V, et al. The association of depressive, anxiety, and stress symptoms andpostpartum relapse to smoking: A longitudinal study. Nicotine & Tobacco Research. 2009;11:707–714. [PubMed: 19436040]

20. Carmichael SL, Ahluwalia IB. Correlates of postpartum smoking relapse: Results from thepregnancy risk assessment monitoring system (PRAMS). American Journal of PreventiveMedicine. 2000; 19:193–196. [PubMed: 11020597]

21. Van't Hof SM, Wall MA, Dowler DW, Stark MJ. Randomised controlled trial of a postpartumrelapse prevention intervention. Tobacco Control. 2000; 9:iii64–iii66. [PubMed: 10982911]

22. Mullen PD, Richardson MA, Quinn VP, Ershoff DH. Postpartum return to smoking: Who is at riskand when. American Journal of Health Promotion. 1997; 11:323–330. [PubMed: 10167366]

Businelle et al. Page 11

Ann Behav Med. Author manuscript; available in PMC 2014 April 01.

NIH

-PA Author Manuscript

NIH

-PA Author Manuscript

NIH

-PA Author Manuscript

23. Gallo LC, Matthews KA. Understanding the association between socioeconomic status andphysical health: Do negative emotions play a role? Psychological Bulletin. 2003; 129:10–51.[PubMed: 12555793]

24. Adler NE, Ostrove JM. Socioeconomic status and health: What we know and what we don't.Annals of the New York Academy of Sciences. 1999; 896:3–15. [PubMed: 10681884]

25. Kendzor DE, Businelle MS, Mazas CA, et al. Pathways between socioeconomic status and healthbehavior among African American smokers. Journal of Behavioral Medicine. 2009; 32:545–557.[PubMed: 19757014]

26. Matthews KA, Gallo LC, Taylor SE. Are psychosocial factors mediators of socioeconomic statusand health connections? A progress report and blueprint for the future. Annals of New YorkAcademy of Sciences. 2010; 1186:146–173.

27. Ritter C, Hobfoll SE, Lavin J, Cameron RP, Hulsizer MR. Stress, psychosocial resources, anddepressive symptomatology during pregnancy in low-income, inner-city women. HealthPsychology. 2000; 19:576–585. [PubMed: 11129361]

28. Witkiewitz K, Marlatt GA. Relapse prevention for alcohol and drug problems: That was Zen, thisis Tao. American Psychologist. 2004; 59:224–235. [PubMed: 15149263]

29. Businelle MS, Kendzor DE, Costello TJ, et al. Mechanisms linking socioeconomic status tosmoking cessation: A structural equation modeling approach. Health Psychology. 2010; 29:262–273. [PubMed: 20496980]

30. Killen JD, Fortmann SP. Craving Is Associated With Smoking Relapse: Findings From ThreeProspective Studies. Experimental and Clinical Psychopharmacology. 1997; 5:137–142. [PubMed:9234050]

31. Doherty K, Kinnunen T, Militello F, Garvey A. Urges to smoke during the first month ofabstinence: relationship to relapse and predictors. Psychopharmacology. 1995; 119:171–178.[PubMed: 7659764]

32. Gallo, LC.; Matthews, KA. Do negative emotions mediate the association between socioeconomicstatus and health?. In: Adler, NE.; Marmot, M.; McEwen and, BS.; Stewart, J., editors.Socioeconomic Status and Health in Industrial Nations: Social, Psychological, and BiologicalPathways. New York: New York Academy of Science; 1999.

33. Reitzel LR, Vidrine JI, Businelle MS, et al. Preventing postpartum smoking relapse among diverse,low income women: A randomized clinical trial. Nicotine & Tobacco Research. 2010; 12:326–335. [PubMed: 20154055]

34. Fiore, MC.; Jaen, CR.; Baker, TB., et al. Treating Tobacco Use and Dependence: 2008 Update.Clinical Practice Guideline. Rockville, MD: Department of Health and Human Services. PublicHealth Service; 2008.

35. Watson D, Clark LA, Tellegen A. Development and validation of brief measures of positive andnegative affect: The PANAS scales. Journal of Personality & Social Psychology. 1988; 54:1063–1070. [PubMed: 3397865]

36. Radloff LS. The CES-D scale: A self-report depression scale for research in the general population.Applied Psychological Measurement. 1977; 1:385–401.

37. Cohen, Kamarck T, Mermelstein R. A gobal measure of perceived stress. Journal of Health andSocial Behavior. 1983; 24:385–396. [PubMed: 6668417]

38. Velicer WF, Diclemente CC, Rossi JS, Prochaska JO. Relapse situations and self-efficacy: Anintegrative model. Addictive Behaviors. 1990; 15:271–283. [PubMed: 2378287]

39. Wetter DW, Brandon TH, Baker TB. The relation of affective processing measures and smokingmotivation indices among college-age smokers. Advances in Behaviour Research & Therapy.1992; 14:169–193.

40. Welsch SK, Smith SS, Wetter DW, et al. Development and validation of the Wisconsin SmokingWithdrawal Scale. Experimental & Clinical Psychopharmacology. 1999; 7:354–361. [PubMed:10609970]

41. Muthén, LK.; Muthén, BO. Mplus User's Guide. 5th Edition. Los Angeles, CA: Muthén &Muthén; 2007.

Businelle et al. Page 12

Ann Behav Med. Author manuscript; available in PMC 2014 April 01.

NIH

-PA Author Manuscript

NIH

-PA Author Manuscript

NIH

-PA Author Manuscript

42. Kendzor DE, Cofta-Woerpel LM, Mazas CA, et al. Socioeconomic status, negative affect, andmodifiable cancer risk factors in African-American smokers. Cancer Epidemiology, Biomarkers &Prevention. 2008; 17:2546–2554.

43. Webb MS, de Ybarra DR, Baker EA, Reis IM, Carey MP. Cognitive-behavioral therapy topromote smoking cessation among African American smokers: a randomized clinical trial. Journalof Consulting & Clinical Psychology. 2010; 78:24–33. [PubMed: 20099947]

44. Swan GE, McClure JB, Jack LM, et al. Behavioral counseling and varenicline treatment forsmoking cessation. American Journal of Preventive Medicine. 2010; 38:482–490. [PubMed:20409497]

45. Bentler PM. Comparative fit indexes in structural models. Psychological Bulletin. 1990; 107:238–246. [PubMed: 2320703]

46. Hu L, Bentler PM. Fit indices in covariance structure modeling: Sensitivity to underparameterizedmodel misspecification. Psychological Methods. 1998; 3:424–453.

47. Browne, MW.; Cudeck, R. Alternative ways of assessing model fit. In: Bollen, KA.; Long, JS.,editors. Testing Structural Equation Models. Beverly Hills, CA: Sage; 1993. p. 136-162.

48. Yu, CY.; Muthén, B. Evaluation of model fit indices for latent variable models with categoricaland continuous outcomes (Technical Report). Los Angeles: University of California at LosAngeles, Graduate School of Education and Information Studies; 2002.

49. Brown, TA. Confirmatory Factor Analysis for Applied Research. New York: Guilford Press; 2006.

50. Tucker LR, Lewis C. A reliability coefficient for maximum likelihood factor analysis.Psychometrika. 1973; 38:1–10.

51. Steiger JH. Structural model equation and modification: An interval estimation approach.Multivariate Behavioral Research. 1990; 25

52. Schwarz G. Estimating the Dimension of a Model. The Annals of Statistics. 1978; 6:461–464.

53. Kass RE, Raftery AE. Bayes Factors. Journal of the American Statistical Association. 1995;90:773–795.

54. Raftery AE. Bayesian model selection in social research. Sociological Methodology. 1995;25:111–163.

55. Siahpush M, McNeill A, Borland R, Fong GT. Socioeconomic variations in nicotine dependence,self-efficacy, and intention to quit across four countries: findings from the International TobaccoControl (ITC) Four Country Survey. Tobacco Control. 2006; 15:iii71–iii75. [PubMed: 16754950]

56. Jarvis, MJ.; Wardle, J. Social patterning of individual health behaviours: The case of cigarettesmoking. In: Marmot, M.; Wilkinson, RG., editors. Social determinants of health. Oxford,England: Oxford University Press; 1999.

57. Hyland A, Li Q, Bauer JE, et al. Predictors of cessation in a cohort of current and former smokersfollowed over 13 years. Nicotine & Tobacco Research. 2004; 6:S363–S369. [PubMed: 15799599]

58. Killen JD, Fortmann SP, Kraemer HC, Varady A, Newman B. Who will relapse? Symptoms ofnicotine dependence predict long-term relapse after smoking cessation. J Consult Clin Psychol.1992; 60:797–801. [PubMed: 1401396]

59. Polanska K, Hanke W, Sobala W, Lowe J, Jaakkola JK. Predictors of Smoking Relapse AfterDelivery: Prospective Study in Central Poland. Maternal and Child Health Journal. 2011; 15:579–586. [PubMed: 20623367]

60. Lemola S, Grob A. Smoking cessation during pregnancy and relapse after childbirth: the impact ofthe grandmother's smoking status. Matern Child Health J. 2008; 12:525–533. [PubMed:17680214]

61. Ma Y, Goins K, Pbert L, Ockene J. Predictors of Smoking Cessation in Pregnancy andMaintenance Postpartum in Low-Income Women. Maternal and Child Health Journal. 2005;9:393–402. [PubMed: 16220356]

62. Fang WL, Goldstein AO, Butzen AY, et al. Smoking cessation in pregnancy: A review ofpostpartum relapse prevention strategies. Journal of the American Board of Family Practice. 2004;17:264–275. [PubMed: 15243014]

63. Manfredi C, Cho YI, Crittenden KS, Dolecek TA. A path model of smoking cessation in womensmokers of low socio-economic status. Health Education Research. 2007; 22:747–756. [PubMed:17182971]

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-PA Author Manuscript

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-PA Author Manuscript

64. Ullman JB. Structural equation modeling: Reviewing the basics and moving forward. Journal ofPersonality Assessment. 2006; 87:35–50. [PubMed: 16856785]

65. Coleman-Cowger V. Smoking Cessation Intervention for Pregnant Women: A Call for Extensionto the Postpartum Period. Maternal and Child Health Journal. 2011:1–4. [PubMed: 20824316]

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Figure 1.Structural equation models of the relation between SES and relapse status.

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Figure 2.Standardized path coefficients and factor loadings for Model 1.SES = Socioeconomic Status; PANAS NA = Positive and Negative Affect Scale-NegativeAffect; PSS = Perceived Stress Scale; CES-D = Center of Epidemiologic Studies DepressionScale; AIPQ = Affective Information Processing Questionnaire.0 = continuous abstinence, 1 = relapsed; 0 = usual care, 1 = MAPS.Solid paths are significant at the p < .05 level, dotted paths are not significant.

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Figure 3.Standardized path coefficients and factor loadings for Model 2.SES = Socioeconomic Status; PANAS NA = Positive and Negative Affect Scale-NegativeAffect; PSS = Perceived Stress Scale; CES-D = Center of Epidemiologic Studies DepressionScale; AIPQ = Affective Information Processing Questionnaire.0 = continuous abstinence, 1 = relapsed; 0 = usual care, 1 = MAPS.Solid paths are significant at the p < .05 level, dotted paths are not significant.

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Table 1

Participant Characteristics

Variable Mean (SD)

Positive and Negative Affect Scale-Negative Affect 21.71 (8.33)

Perceived Stress Scale 6.47 (3.14)

Center of Epidemiologic Studies Depression Scale 18.23 (11.33)

Self-Efficacy/Confidence Scale

Positive Affect 3.74 (0.98)

Negative Affect 3.38 (1.19)

Habit/Craving 4.18 (0.84)

Affective Information Processing Questionnaire 5.05 (1.33)

Wisconsin Smoking Withdrawal Scale

Urge 1.39 (1.29)

Thoughts 1.32 (1.24)

Desire 1.47 (1.31)

Focus 0.83 (1.02)

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Tabl

e 2

Zer

o O

rder

Cor

rela

tions

12

34

56

78

910

1112

1314

SES

1. E

duca

tion

-

2. E

mpl

oym

ent1

.401

***

-

3. I

ncom

e.5

20**

*.3

43**

*-

Aff

ect/S

tres

s

4. P

AN

AS

NA

−.0

21−

.013

−.0

59-

5. P

SS−

.154

*−

.094

−.1

82**

.655

***

-

6. C

ES-

D−

.209

***

−.1

14−

.234

***

.579

***

.518

***

-

Age

ncy

7. P

ositi

ve a

ffec

t−

.078

−.0

76−

.066

−.2

93**

*−

.213

***

−.2

05**

*-

8. N

egat

ive

affe

ct−

.039

.058

.013

−.3

14**

*−

.239

***

−.2

41**

*.7

43**

*-

9. H

abit/

crav

ing

.071

.062

.125

−.3

47**

*−

.269

***

−.2

98**

*.7

62**

*.7

25**

*-

10. A

IPQ

.060

.020

.064

−.2

70**

*−

.259

***

−.2

33**

*.4

20**

*.4

49**

*.5

05**

*-

Cra

ving

11. U

rges

−.0

51−

.059

−.0

39.3

55**

*.3

63**

*.2

29**

*−

.362

***

−.3

26**

*−

.360

***

−.2

08**

*-

12. T

houg

hts

−.0

61−

.038

−.0

13.2

73**

*.3

05**

*.1

88**

−.3

46**

*−

.286

***

−.3

64**

*−

.253

***

.683

***

-

13. D

esir

e−

.016

.007

.063

.237

***

.270

***

.137

*−

.317

***

−.3

01**

*−

.328

***

−.2

05**

*.6

17**

*.6

34**

*-

14. F

ocus

−.0

72−

.038

−.0

12.3

05**

*.3

25**

*.2

19**

*−

.420

***

−.3

80**

*−

.434

***

−.2

62**

*.5

27**

*.6

75**

*.5

42**

*-

Rel

apse

Sta

tus

15. W

eek

82−

.148

*−

.129

*−

.128

.066

.145

*.1

29*

−.1

92**

−.2

40**

*−

.191

**−

.134

*.2

03**

*.3

06**

*.1

96**

.276

***

* p <

.05;

**p

< .0

1;

*** p

< .0

01;

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Businelle et al. Page 201 0

= u

nem

ploy

ed, 1

= e

mpl

oyed

;

2 0 =

con

tinuo

us a

bstin

ence

, 1 =

rel

apse

d.

SES

= S

ocio

econ

omic

Sta

tus;

PA

NA

S N

A =

Pos

itive

and

Neg

ativ

e A

ffec

t Sca

le-N

egat

ive

Aff

ect;

PSS

= P

erce

ived

Str

ess

Scal

e; C

ES-

D =

Cen

ter

of E

pide

mio

logi

c St

udie

s D

epre

ssio

n Sc

ale;

AIP

Q =

Aff

ectiv

e In

form

atio

n Pr

oces

sing

Que

stio

nnai

re.

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Table 3

Standardized Indirect and Total Effects of Predictors of Smoking Relapse at 8 Weeks Postpartum

Model 1 Model 2

Variable Indirect Total Indirect Total

Socioeconomic Status −0.02* −0.24 −0.04 −0.26

Negative Affect/Stress 0.09 0.09 0.19 0.19

Agency - −0.41 −0.20 −0.20

Craving 0.25 0.25 - 0.43

Note: All indirect and total effects are significant at the p < .05 level;

*p = .057

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